Evidence for Biological Age Acceleration and Telomere Shortening in COVID-19 Survivors

• Main Authors: Alessia Mongelli, Veronica Barbi, Michela Gottardi Zamperla, Sandra Atlante, Luana Forleo, Marialisa Nesta, Massimo Massetti, Alfredo Pontecorvi, Simona Nanni, Antonella Farsetti, Oronzo Catalano, Maurizio Bussotti, Laura Adelaide Dalla Vecchia, Tiziana Bachetti, Fabio Martelli, Maria Teresa La Rovere, Carlo Gaetano
• Format: Article
• Language: English
• Published: MDPI AG 2021-06-01
• Series: International Journal of Molecular Sciences
• Subjects: biological age; COVID-19; post-COVID-19; telomeres; epigenetics; DNA methylation
• Online Access: https://www.mdpi.com/1422-0067/22/11/6151
• ISSN: 1661-6596; 1422-0067

The SARS-CoV-2 infection determines the COVID-19 syndrome characterized, in the worst cases, by severe respiratory distress, pulmonary and cardiac fibrosis, inflammatory cytokine release, and immunosuppression. This condition has led to the death of about 2.15% of the total infected world population so far. Among survivors, the presence of the so-called persistent post-COVID-19 syndrome (PPCS) is a common finding. In COVID-19 survivors, PPCS presents one or more symptoms: fatigue, dyspnea, memory loss, sleep disorders, and difficulty concentrating. In this study, a cohort of 117 COVID-19 survivors (post-COVID-19) and 144 non-infected volunteers (COVID-19-free) was analyzed using pyrosequencing of defined CpG islands previously identified as suitable for biological age determination. The results show a consistent biological age increase in the post-COVID-19 population, determining a DeltaAge acceleration of 10.45 ± 7.29 years (+5.25 years above the range of normality) compared with 3.68 ± 8.17 years for the COVID-19-free population (<i>p</i> < 0.0001). A significant telomere shortening parallels this finding in the post-COVID-19 cohort compared with COVID-19-free subjects (<i>p</i> < 0.0001). Additionally, ACE2 expression was decreased in post-COVID-19 patients, compared with the COVID-19-free population, while DPP-4 did not change. In light of these observations, we hypothesize that some epigenetic alterations are associated with the post-COVID-19 condition, particularly in younger patients (< 60 years).